In a normal human heart, the sinus node, generally located near the junction of the superior vena cava and the right atrium, constitutes the primary natural pacemaker initiating rhythmic electrical excitation of the heart chambers. The cardiac impulse arising from the sinus node is transmitted to the two atrial chambers, causing a depolarization known as a P-wave and the resulting atrial chamber contractions. The excitation pulse is further transmitted to and through the ventricles via the atrioventricular (A-V) node and a ventricular conduction system causing a depolarization known as an R-wave and the resulting ventricular chamber contractions.
Disruption of this natural pacing and conduction system as a result of aging or disease can be successfully treated by artificial cardiac pacing using implantable cardiac stimulation devices, including pacemakers and implantable defibrillators, which deliver rhythmic electrical pulses or other anti-arrhythmia therapies to the heart, via electrodes implanted in contact with the heart tissue, at a desired energy and rate. One or more heart chambers may be electrically stimulated depending on the location and severity of the conduction disorder.
A single-chamber pacemaker delivers pacing pulses to one chamber of the heart, either one atrium or one ventricle. Dual chamber pacemakers are now commonly available and can provide stimulation in both an atrial chamber and a ventricular chamber, typically the right atrium and the right ventricle. Both unipolar or bipolar dual chamber pacemakers exist in which a unipolar or bipolar lead extends from an atrial channel of the dual chamber device to the desired atrium (e.g. the right atrium), and a separate unipolar or bipolar lead extends from a ventricular channel to the corresponding ventricle (e.g. the right ventricle). In dual chamber, demand-type pacemakers, commonly referred to as DDD pacemakers, each atrial and ventricular channel includes a sense amplifier to detect cardiac activity in the respective chamber and an output circuit for delivering stimulation pulses to the respective chamber.
If an intrinsic atrial depolarization signal (a P-wave) is not detected by the atrial channel, a stimulating pulse will be delivered to depolarize the atrium and cause contraction. Following either a detected P-wave or an atrial pacing pulse, the ventricular channel attempts to detect a depolarization signal in the ventricle, known as an R-wave. If no R-wave is detected within a defined atrial-ventricular interval (AV interval, also referred to as AV delay), a stimulation pulse is delivered to the ventricle to cause ventricular contraction. In this way, atrioventricular synchrony is achieved by coordinating the delivery of ventricular output in response to a sensed or paced atrial event.
Unfortunately, a pacemaker operating in the DDD mode may contribute, in combination with other factors, to a pacemaker-mediated tachycardia (PMT). For example, in patients who are prone to atrial arrhythmias, e.g., a fast atrial rate, the DDD pacer tracks the fast atrial rate, causing the ventricles to be paced at a correspondingly fast rate, thereby causing a tachycardia (fast heart rate) to occur. Without the DDD pacemaker, such tachycardia would probably not occur because the ventricles would normally continue at a slower (more normal) rate, despite the fast atrial rate. However, with the DDD pacemaker, the stimulation of the ventricles occurs so as to track the fast atrial rate, and thus the pacemaker effectively intervenes or “mediates” so as to cause the tachycardia, appropriately termed a “pacemaker-mediated tachycardia,” or PMT, to occur.
There are other reasons why a pacemaker-mediated tachycardia may be triggered by a DDD pacer, other than simply tracking a fast atrial rate. For example, prolonged intervals between atrial and ventricular depolarization can cause or enhance retrograde conduction of the depolarization wave back into the atria producing what is referred to as a “retrograde P-wave.” A retrograde P-wave may be sensed by the atrial channel sensing circuits. Unfortunately, the pacemaker sensing circuits cannot differentiate between retrograde P-waves and normal P-waves, so such sensing may result in a pacemaker-mediated tachycardia wherein each ventricular paced event is followed by a retrograde P-wave which is tracked, resulting in another ventricular paced event, causing the process to repeat.
It is well known that the type of pacemaker-mediated tachycardia described above (resulting from sensing retrograde P-waves) can be prevented by programming the post ventricular atrial refractory period (PVARP) of the pacemaker to be longer than the retrograde conduction time. Such lengthening of the PVARP, however, disadvantageously prevents the sensing of a P-wave that occurs late in the PVARP. A failure to sense a P-wave, in turn, causes an atrial stimulus to be generated by the pacemaker that is more than likely delivered into the heart's atrial refractory period, at a time when such pulse is ineffective. This results in an effective prolongation of the P-to-V interval, which may either decrease hemodynamic performance and/or induce retrograde conduction. Even worse, the possibility exists that the atrial stimulus (delivered into the heart during the atrial refractory period) may induce atrial flutter or fibrillation.
Several approaches are known in the art to minimize the likelihood of a pacemaker-mediated tachycardia caused by the sensing of retrograde P-waves in patients having a dual-chamber pacing system. For example, a maximum tracking rate may be incorporated in modern DDD pacemakers. Another approach is Automatic Mode Switch that switches the pacing mode from any tracking mode (DDD or VDD) to a non-tracking mode. If the natural atrial rate exceeds this maximum tracking rate, the pacemaker converts to a non-tracking mode (known as a DDI mode). Sensing continues in both the atrium and the ventricle, but the ventricle is stimulated at a rate independent of the high atrial rate. If the atrial rate decreases again, the pacemaker may convert back to the DDD mode.
In order to detect pacemaker-mediated tachycardia, the time between the ventricular stimulation pulse and a sensed P-wave may be measured. If a short, stable interval is measured, the sensed P-wave is suspected of being a retrograde P-wave. Corrective action may then be taken to terminate the pacemaker-mediated tachycardia, for example converting to an atrial non-tracking mode such as DDI.
Mounting clinical evidence supports the evolution of more complex cardiac stimulating devices capable of stimulating three or even all four heart chambers to stabilize arrhythmias or to re-synchronize heart chamber contractions (Ref: Cazeau S., “Four chamber pacing in dilated cardiomyopathy,” Pacing Clin. Electrophsyiol 1994 17(11 Pt 2):1974–9). Stimulation of multiple sites within a heart chamber has also been found effective in controlling arrhythmogenic depolarizations (Ref: Ramdat-Misier A., “Multisite or alternate site pacing for the prevention of atrial fibrillation,” Am. J. Cardiol., 1999 11;83(5b):237D–240D). In these multi-site or multi-chamber stimulation applications, correct synchronization of all heart chambers is vital to achieving a desired hemodynamic benefit. However, the occurrence of retrograde P-waves during biventricular or multi-site ventricular stimulation may lead to pacemaker-mediated tachycardia in the same way as described for dual chamber pacemakers. Retrograde P-waves may arise from more than one ventricular stimulation site. Therefore, in multi-site and multi-chamber stimulation devices, detection of retrograde P-waves and prevention of pacemaker-mediated tachycardia is just as important as in dual chamber devices.
The ability to detect the presence of retrograde P-waves during stimulation of more than one site within the ventricles, however, becomes more complex than in dual chamber stimulation because the retrograde P-waves may be arising from more than one retrograde pathway, each with a different conduction time. Sensed retrograde P-waves will increase the detected atrial rate indicating an atrial tachycardia when in fact there is none causing the stimulation device to deliver or withhold stimulation inappropriately. Sensed retrograde P-waves may also induce pacemaker-mediated tachycardia. Both of these situations are highly undesirable. What is needed, therefore, is a method for detecting retrograde P-waves during biventricular or multi-site ventricular stimulation and determining the site of ventricular stimulation associated with the retrograde conduction.